Antioxidant activity and inhibition of human neutrophil oxidative burst mediated by arylpropionic acid non-steroidal anti-inflammatory drugs

It has been suggested that the anti-inflammatory activity of some non-steroidal anti-inflammatory drugs (NSAIDs) may be partly due to their ability to scavenge reactive oxygen species (ROS) and reactive nitrogen species (RNS), as well as to inhibit the respiratory burst of neutrophils triggered by various activating agents. Therefore, the aim of the present work was to evaluate and compare the potential scavenging activity for an array of ROS (O-2(center dot-), H2O2, HO center dot, ROO center dot and HOCl) and RNS ((NO)-N-center dot and ONOO-) using in vitro non-cellular screening systems as well as a cellular screening system (human neutrophil oxidative burst), mediated by the arylpropionic acid derivatives (APAs) NSAIDs ibuprofen, flurbiprofen, fenoprofen, fenbufen, ketoprofen, naproxen and indoprofen. The results obtained in the present work demonstrate that under the present experimental conditions, many of the studied APA NSAIDs showed O-2(center dot-) scavenging activity (fenbufen approximate to flurbiprofen approximate to indoprofen approximate to ketoprofen), H2O2 (ketoprofen approximate to indoprofen approximate to fenbufen > flurbiprofen > naproxen), HO center dot (fenoprofen approximate to ibuprofen > fenbufen approximate to flurbiprofen > ketoprofen > indoprofen approximate to naproxen), (NO)-N-center dot (indoprofen > naproxen), ONOO- (indoprofen > naproxen > fenoprofen approximate to flurbiprofen approximate to ibuprofen), as well as inhibit myeloperoxidase (MPO) activity (indoprofen) and scavenge human neutrophil derived ROS (ketoprofen > indoprofen > fenbufen > flurbiprofen). The observed effects, if confirmed in vivo, may strongly contribute to the anti-inflammatory therapeutical activity observed with these NSAIDs.